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polyclonal anti alk2 antibody (R&D Systems)

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R&D Systems polyclonal anti alk2 antibody
Polyclonal Anti Alk2 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 10 article reviews

polyclonal anti alk2 antibody - by Bioz Stars, 2026-05

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Figure 6. Receptor expressions of ALK2, ALK4, ALK6, ALK5, ALK7, BMPR-II in pASC. Grouped representation of the respective receptor expression in the course of osteogenic differentiation (OM +/−BMP-2). From day 19, there is a significant induction of ALK 2, ALK 6, and ALK 5 with the addition of BMP-2. BMPR-II expression in the OM group decreased in OM and tended to stay increased under BMP-2 supplementation from day 19, but was not considered significant (* p ≤0.05, ** p ≤0.01; n = 6, BMP-2 450 ng/mL).

Journal: Biology

Article Title: BMP-2-Driven Osteogenesis: A Comparative Analysis of Porcine BMSCs and ASCs and the Role of TGF-β and FGF Signaling.

doi: 10.3390/biology14060610

Figure Lengend Snippet: Figure 6. Receptor expressions of ALK2, ALK4, ALK6, ALK5, ALK7, BMPR-II in pASC. Grouped representation of the respective receptor expression in the course of osteogenic differentiation (OM +/−BMP-2). From day 19, there is a significant induction of ALK 2, ALK 6, and ALK 5 with the addition of BMP-2. BMPR-II expression in the OM group decreased in OM and tended to stay increased under BMP-2 supplementation from day 19, but was not considered significant (* p ≤0.05, ** p ≤0.01; n = 6, BMP-2 450 ng/mL).

Article Snippet: The respective conjugated antibodies were used for the expressions of ALK3 (Cat. No.: AF436), ALK 5 (Cat. No.: FAB5871), ALK6 (Cat. No.: FAB5051A), TGF-β2-RII (Cat. No.: FAB532P), ALK7 (Cat. No.: FAB77491A), ALK2 (Cat. No.: AF637), ALK4 (Cat. No.: MAB2221), and BMPR-II (Cat. No.: AF811) (by R&D Systems, Minneapolis, MN, USA), and the pASCs and pBMSCs were compared for their expressions of the specific surface antigens CD45 (Cat. No.: MCA1568GA, BioRad, Hercules, CA, USA), HLA-DR (human leukocyte antigen–antigen D-related surface molecule) (Cat. No.: MCA2314F, Bio-Rad, Hercules, CA, USA), CD29 (Cat. No.: 561,496, BD Pharmingen, Franklin Lakes, NJ, USA), CD79alpha (Bio-Rad, Cat. No.: MCA2538GA), CD14 (Cat. No.: MCA1568GA, Bio-Rad, Hercules, CA, USA), CD31 (Cat. No.: AF3387, R&D Systems, Minneapolis, MN, USA), CD105 (Cat. No.: NB110-58718APC, Novus Biologicals, Minneapolis, MN, USA), CD26 (, Cat. No.: NB600-552APC, Novus Biologicals, Minneapolis, MN, USA), CD73 (, Cat. No.: AF4488, R&D Systems, Minneapolis, MN, USA), CD90 (Cat. No.: 559,869, BD Pharmingen, Franklin Lakes, NJ, USA), CD34 (Cat. No.: 81289, abcam, Cambridge, UK), and CD44 (Cat. No.: 5531, BD Pharmingen, Franklin Lakes, NJ, USA).

Techniques: Expressing

( A ) Mouse C2C12 myoblast cells express similar levels of Acvr1 and Alk3 , low levels of Alk1 , and no detectable Alk6 , as quantified by RT-qPCR ( n = 3). ΔCT values were calculated using the average CT values of the internal controls, Gapdh or Actb (β-actin) (see Methods). Error bars represent ±SD. CT values >40 were considered not detected (N.D.). ( B ) Surface expression of ACVR1 and ALK3 on C2C12 cells, as detected by flow cytometry. ( C ) mAb JAB0505 binds to parental C2C12 cells, but not Acvr1 -KO cells, as assessed by flow cytometry. ( D ) JAB0505 inhibits BMP9-induced signal activation in wild-type and ACVR1(R206H)-overexpressing C2C12 cells in a dose-dependent manner, as determined by quantification of BRE-luciferase activity ( n = 3). Error bars represent ±SD.

Journal: The Journal of Clinical Investigation

Article Title: An anti-ACVR1 antibody exacerbates heterotopic ossification by fibro-adipogenic progenitors in fibrodysplasia ossificans progressiva mice

doi: 10.1172/JCI153795

Figure Lengend Snippet: ( A ) Mouse C2C12 myoblast cells express similar levels of Acvr1 and Alk3 , low levels of Alk1 , and no detectable Alk6 , as quantified by RT-qPCR ( n = 3). ΔCT values were calculated using the average CT values of the internal controls, Gapdh or Actb (β-actin) (see Methods). Error bars represent ±SD. CT values >40 were considered not detected (N.D.). ( B ) Surface expression of ACVR1 and ALK3 on C2C12 cells, as detected by flow cytometry. ( C ) mAb JAB0505 binds to parental C2C12 cells, but not Acvr1 -KO cells, as assessed by flow cytometry. ( D ) JAB0505 inhibits BMP9-induced signal activation in wild-type and ACVR1(R206H)-overexpressing C2C12 cells in a dose-dependent manner, as determined by quantification of BRE-luciferase activity ( n = 3). Error bars represent ±SD.

Article Snippet: Clones were screened for ACVR1 or ALK3 protein expression by flow cytometry with an anti-ACVR1 antibody (R&D Systems, AF637) and an anti-ALK3 antibody (Sino Biological, 50078), respectively.

Techniques: Quantitative RT-PCR, Expressing, Flow Cytometry, Activation Assay, Luciferase, Activity Assay

( A ) Representative μCT images of HO in Acvr1 FLEx(R206H)/+ ; CAG-Cre ERT2 mice 20 days after cardiotoxin-induced injury of the gastrocnemius muscle (Untreated, n = 3; JAB0505, n = 4). ( B ) Representative μCT images of HO (pseudocolored green) in Acvr1 tnR206H/+ ; Tie2-Cre mice 21 days after pinch injury of the gastrocnemius muscle (Untreated, n = 11; JAB0505, n = 10). ( C ) Quantification of HO volumes as a function of time after muscle pinch injury of Acvr1 tnR206H/+ ; Tie2-Cre mice. Untreated, n = 11; JAB0505 (10 mg/kg), n = 6. Error bars represent ±SEM. **** P ≤ 0.0001 by 2-way ANOVA with Sidak’s multiple-comparison test. ( D ) Paired single transverse slice and 3D reconstructed μCT images of the distal hind limb of Acvr1 tnR206H/+ ; Tie2-Cre mice at the indicated times after hind limb muscle pinch injury with and without administration of JAB0505. Mineralized bone in the slice images is pseudocolored green. Radio-opaque lesional tissue below the threshold set for quantification of mineralized bone (white arrows in day 14 slices) is extensive at day 14 in JAB0505-treated mice. Mineralized bone in day 14 slices is barely visible at this magnification. HO volumes are given for images prior to day 35. The tibia and fibula are labeled with asterisks in the day 14 slices. Pelvic bones present in day 21, 28, and 35 slices of JAB0505-treated mice are denoted with arrowheads. To avoid confusion with HO, the baculum present in some images was removed by segmentation.

Journal: The Journal of Clinical Investigation

Article Title: An anti-ACVR1 antibody exacerbates heterotopic ossification by fibro-adipogenic progenitors in fibrodysplasia ossificans progressiva mice

doi: 10.1172/JCI153795

Figure Lengend Snippet: ( A ) Representative μCT images of HO in Acvr1 FLEx(R206H)/+ ; CAG-Cre ERT2 mice 20 days after cardiotoxin-induced injury of the gastrocnemius muscle (Untreated, n = 3; JAB0505, n = 4). ( B ) Representative μCT images of HO (pseudocolored green) in Acvr1 tnR206H/+ ; Tie2-Cre mice 21 days after pinch injury of the gastrocnemius muscle (Untreated, n = 11; JAB0505, n = 10). ( C ) Quantification of HO volumes as a function of time after muscle pinch injury of Acvr1 tnR206H/+ ; Tie2-Cre mice. Untreated, n = 11; JAB0505 (10 mg/kg), n = 6. Error bars represent ±SEM. **** P ≤ 0.0001 by 2-way ANOVA with Sidak’s multiple-comparison test. ( D ) Paired single transverse slice and 3D reconstructed μCT images of the distal hind limb of Acvr1 tnR206H/+ ; Tie2-Cre mice at the indicated times after hind limb muscle pinch injury with and without administration of JAB0505. Mineralized bone in the slice images is pseudocolored green. Radio-opaque lesional tissue below the threshold set for quantification of mineralized bone (white arrows in day 14 slices) is extensive at day 14 in JAB0505-treated mice. Mineralized bone in day 14 slices is barely visible at this magnification. HO volumes are given for images prior to day 35. The tibia and fibula are labeled with asterisks in the day 14 slices. Pelvic bones present in day 21, 28, and 35 slices of JAB0505-treated mice are denoted with arrowheads. To avoid confusion with HO, the baculum present in some images was removed by segmentation.

Techniques: Comparison, Labeling

( A ) Transverse sections of muscle from untreated and JAB0505-treated Acvr1 tnR206H/+ ; Tie2-Cre mice on days 6 and 14 after muscle pinch injury. Alcian blue staining to detect cartilage (blue) and immunohistochemical staining to detect ACVR1 (brown) were performed on nearby sections. Sections processed for Alcian blue were counterstained with eosin, and sections processed for ACVR1 immunohistochemistry were counterstained with hematoxylin. On day 6 after injury, untreated Acvr1 tnR206H/+ ; Tie2-Cre mice exhibited a spatially discrete lesional region (asterisk) that was primarily comprised of ACVR1-positive ectopic cartilage. By day 14, the lesional region (asterisk) of untreated Acvr1 tnR206H/+ ; Tie2-Cre mice displayed sporadic ACVR1 localization and was composed of both cartilage and morphologically apparent bone. In contrast, JAB0505 treated Acvr1 tnR206H/+ ; Tie2-Cre mice displayed multiple apparent cartilaginous lesions and broader distribution of ACVR1 localization on days 6 and 14 (arrows). Centrally located myofiber nuclei (arrowheads), which identify regenerated fibers, were rare in Acvr1 tnR206H/+ ; Tie2-Cre mice, and undetected in JAB0505-treated Acvr1 tnR206H/+ ; Tie2-Cre mice. AB/E, Alcian blue/eosin. Original magnification, ×100. ( B ) Transverse sections of lower hind limbs of Acvr1 tnR206H/+ ; Tie2-Cre mice 14 days after injury. Alcian blue staining revealed numerous cartilaginous lesions (blue, examples at arrows) in injured muscle of JAB0505-treated mice. Sections were counterstained with eosin. T, tibia. Original magnification, ×40.

Journal: The Journal of Clinical Investigation

Article Title: An anti-ACVR1 antibody exacerbates heterotopic ossification by fibro-adipogenic progenitors in fibrodysplasia ossificans progressiva mice

doi: 10.1172/JCI153795

Figure Lengend Snippet: ( A ) Transverse sections of muscle from untreated and JAB0505-treated Acvr1 tnR206H/+ ; Tie2-Cre mice on days 6 and 14 after muscle pinch injury. Alcian blue staining to detect cartilage (blue) and immunohistochemical staining to detect ACVR1 (brown) were performed on nearby sections. Sections processed for Alcian blue were counterstained with eosin, and sections processed for ACVR1 immunohistochemistry were counterstained with hematoxylin. On day 6 after injury, untreated Acvr1 tnR206H/+ ; Tie2-Cre mice exhibited a spatially discrete lesional region (asterisk) that was primarily comprised of ACVR1-positive ectopic cartilage. By day 14, the lesional region (asterisk) of untreated Acvr1 tnR206H/+ ; Tie2-Cre mice displayed sporadic ACVR1 localization and was composed of both cartilage and morphologically apparent bone. In contrast, JAB0505 treated Acvr1 tnR206H/+ ; Tie2-Cre mice displayed multiple apparent cartilaginous lesions and broader distribution of ACVR1 localization on days 6 and 14 (arrows). Centrally located myofiber nuclei (arrowheads), which identify regenerated fibers, were rare in Acvr1 tnR206H/+ ; Tie2-Cre mice, and undetected in JAB0505-treated Acvr1 tnR206H/+ ; Tie2-Cre mice. AB/E, Alcian blue/eosin. Original magnification, ×100. ( B ) Transverse sections of lower hind limbs of Acvr1 tnR206H/+ ; Tie2-Cre mice 14 days after injury. Alcian blue staining revealed numerous cartilaginous lesions (blue, examples at arrows) in injured muscle of JAB0505-treated mice. Sections were counterstained with eosin. T, tibia. Original magnification, ×40.

Techniques: Staining, Immunohistochemical staining, Immunohistochemistry

μCT images of the distal hind limbs of 4 Acvr1 tnR206H/+ ; Tie2-Cre FOP mice (numbered 1–4) at the indicated time points after injection of 50 μL of 2.5% methylcellulose into the tibialis anterior muscle, with and without administration of 10 mg/kg JAB0505 ( n = 2 mice, 4 injected limbs, for each group). HO is pseudocolored green. A lateral view of the right hind limb of each mouse is shown. Contralateral hind limbs (not shown) received equivalent injuries and the extent of HO was comparable.

Journal: The Journal of Clinical Investigation

Article Title: An anti-ACVR1 antibody exacerbates heterotopic ossification by fibro-adipogenic progenitors in fibrodysplasia ossificans progressiva mice

doi: 10.1172/JCI153795

Figure Lengend Snippet: μCT images of the distal hind limbs of 4 Acvr1 tnR206H/+ ; Tie2-Cre FOP mice (numbered 1–4) at the indicated time points after injection of 50 μL of 2.5% methylcellulose into the tibialis anterior muscle, with and without administration of 10 mg/kg JAB0505 ( n = 2 mice, 4 injected limbs, for each group). HO is pseudocolored green. A lateral view of the right hind limb of each mouse is shown. Contralateral hind limbs (not shown) received equivalent injuries and the extent of HO was comparable.

Techniques: Injection

( A ) Osteogenic differentiation of monolayer R206H-FAP cultures, as assessed by ALP staining (purple), and ( B ) chondrogenic differentiation of micromass cultures assessed by Alcian blue staining. ActA-mAb was used at 1 μg/mL (7 nM) and JAB0505 was used at 10 μg/mL (~70 nM). ( C ) Western blot of phosphorylated SMAD1/5/8 (p-SMAD1/5/8) in wild-type (WT) and R206H-FAPs (R206H). β-Actin was used as a loading control. ( D ) μCT of the distal hind limb of Acvr1 tnR206H/+ ; Tie2-Cre mice on day 21 after injury. At the time of muscle injury, mice were treated with ActA-mAb (10 mg/kg) alone or ActA-mAb with JAB0505 (10 mg/kg). HO is pseudocolored green, and quantification is shown. ActA-mAb, n = 6; JAB0505 plus ActA-mAb, n = 6. Error bars represent ±SD. **** P < 0.0001 by 2-tailed, unpaired t test. ( E ) μCT images of the distal hind limb 21 days after transplantation of R206H-FAPs into the injured gastrocnemius of SCID hosts. ActA-mAb (10 mg/kg) and JAB0505 (10 mg/kg) were administered at the time of transplantation. HO is pseudocolored green and quantified, with error bars representing ±SD. Untreated, n = 10; JAB0505, n = 16; ActA-mAb, n = 6; JAB0505 plus ActA-mAb, n = 8.

Journal: The Journal of Clinical Investigation

Article Title: An anti-ACVR1 antibody exacerbates heterotopic ossification by fibro-adipogenic progenitors in fibrodysplasia ossificans progressiva mice

doi: 10.1172/JCI153795

Figure Lengend Snippet: ( A ) Osteogenic differentiation of monolayer R206H-FAP cultures, as assessed by ALP staining (purple), and ( B ) chondrogenic differentiation of micromass cultures assessed by Alcian blue staining. ActA-mAb was used at 1 μg/mL (7 nM) and JAB0505 was used at 10 μg/mL (~70 nM). ( C ) Western blot of phosphorylated SMAD1/5/8 (p-SMAD1/5/8) in wild-type (WT) and R206H-FAPs (R206H). β-Actin was used as a loading control. ( D ) μCT of the distal hind limb of Acvr1 tnR206H/+ ; Tie2-Cre mice on day 21 after injury. At the time of muscle injury, mice were treated with ActA-mAb (10 mg/kg) alone or ActA-mAb with JAB0505 (10 mg/kg). HO is pseudocolored green, and quantification is shown. ActA-mAb, n = 6; JAB0505 plus ActA-mAb, n = 6. Error bars represent ±SD. **** P < 0.0001 by 2-tailed, unpaired t test. ( E ) μCT images of the distal hind limb 21 days after transplantation of R206H-FAPs into the injured gastrocnemius of SCID hosts. ActA-mAb (10 mg/kg) and JAB0505 (10 mg/kg) were administered at the time of transplantation. HO is pseudocolored green and quantified, with error bars representing ±SD. Untreated, n = 10; JAB0505, n = 16; ActA-mAb, n = 6; JAB0505 plus ActA-mAb, n = 8.

Techniques: Staining, Western Blot, Control, Transplantation Assay

( A ) 3D tomographic bioluminescence source reconstruction following muscle pinch injury of Acvr1 tnR206H/+ ; R26 Luc/+ ; Tie2-Cre FOP mice, with and without administration of JAB0505. Paired images show μCT alone (left panel) and μCT combined with the corresponding 3D bioluminescence reconstruction (right panel). The same mouse is shown from days 3 to 21. Bioluminescence reconstruction was not performed on day 21 due to the dampening effect of dense bone on luminescent output. ( B ) Graphical representation of bioluminescent population dynamics of Tie2 + cells from Acvr1 tnR206H/+ ; R26 Luc/+ ; Tie2-Cre mice following pinch injury. Untreated, n = 16; JAB0505, n = 10. Error bars represent ±SEM. *** P ≤ 0.001, **** P ≤ 0.0001 by 2-way ANOVA with Sidak’s multiple-comparison test. ( C ) Flow cytometry analysis to determine R206H-FAP cell number in injured distal hind limb muscles of Acvr1 tnR206H/+ ; R26 NG/+ ; Tie2-Cre mice that were either untreated (day 5, n = 4; day 10, n = 9) or administered JAB0505 at 10 mg/kg (day 5, n = 4; day 10, n = 10). Error bars represent ±SD. ** P ≤ 0.01 by 2-tailed, unpaired t test with Welch’s correction.

Journal: The Journal of Clinical Investigation

Article Title: An anti-ACVR1 antibody exacerbates heterotopic ossification by fibro-adipogenic progenitors in fibrodysplasia ossificans progressiva mice

doi: 10.1172/JCI153795

Figure Lengend Snippet: ( A ) 3D tomographic bioluminescence source reconstruction following muscle pinch injury of Acvr1 tnR206H/+ ; R26 Luc/+ ; Tie2-Cre FOP mice, with and without administration of JAB0505. Paired images show μCT alone (left panel) and μCT combined with the corresponding 3D bioluminescence reconstruction (right panel). The same mouse is shown from days 3 to 21. Bioluminescence reconstruction was not performed on day 21 due to the dampening effect of dense bone on luminescent output. ( B ) Graphical representation of bioluminescent population dynamics of Tie2 + cells from Acvr1 tnR206H/+ ; R26 Luc/+ ; Tie2-Cre mice following pinch injury. Untreated, n = 16; JAB0505, n = 10. Error bars represent ±SEM. *** P ≤ 0.001, **** P ≤ 0.0001 by 2-way ANOVA with Sidak’s multiple-comparison test. ( C ) Flow cytometry analysis to determine R206H-FAP cell number in injured distal hind limb muscles of Acvr1 tnR206H/+ ; R26 NG/+ ; Tie2-Cre mice that were either untreated (day 5, n = 4; day 10, n = 9) or administered JAB0505 at 10 mg/kg (day 5, n = 4; day 10, n = 10). Error bars represent ±SD. ** P ≤ 0.01 by 2-tailed, unpaired t test with Welch’s correction.

Techniques: Comparison, Flow Cytometry, Muscles

Flow cytometry analysis was used to determine cell numbers of ( A ) total CD45 + hematopoietic cells, ( B ) myeloid cells, ( C ) lymphoid cells, ( D ) total macrophages, ( E ) Ly6C + inflammatory monocytes/macrophages, ( F ) neutrophils, ( G ) mast cells, and ( H ) T cells in injured distal hind limb muscles of control ( R26 NG/+ ; Tie2-Cre) and FOP ( Acvr1 tnR206H/+ ; R26 NG/+ ; Tie2-Cre) mice that were either untreated or administered 10 mg/kg JAB0505 i.p. ( n = 3–4). Error bars represent ±SD. Significance was determined using 1-way ANOVA with Tukey’s multiple-comparison test within individual time points. Symbols representing significance were placed above FOP and FOP + JAB0505 bars to indicate a comparison to control (^), control + JAB0505 ( # ), and FOP (*). The numbers of symbols of each type denote levels of significance: P ≤ 0.05, P ≤ 0.01, P ≤ 0.001, and P ≤ 0.0001. No control vs. control + JAB0505 comparisons were significant.

Journal: The Journal of Clinical Investigation

Article Title: An anti-ACVR1 antibody exacerbates heterotopic ossification by fibro-adipogenic progenitors in fibrodysplasia ossificans progressiva mice

doi: 10.1172/JCI153795

Figure Lengend Snippet: Flow cytometry analysis was used to determine cell numbers of ( A ) total CD45 + hematopoietic cells, ( B ) myeloid cells, ( C ) lymphoid cells, ( D ) total macrophages, ( E ) Ly6C + inflammatory monocytes/macrophages, ( F ) neutrophils, ( G ) mast cells, and ( H ) T cells in injured distal hind limb muscles of control ( R26 NG/+ ; Tie2-Cre) and FOP ( Acvr1 tnR206H/+ ; R26 NG/+ ; Tie2-Cre) mice that were either untreated or administered 10 mg/kg JAB0505 i.p. ( n = 3–4). Error bars represent ±SD. Significance was determined using 1-way ANOVA with Tukey’s multiple-comparison test within individual time points. Symbols representing significance were placed above FOP and FOP + JAB0505 bars to indicate a comparison to control (^), control + JAB0505 ( # ), and FOP (*). The numbers of symbols of each type denote levels of significance: P ≤ 0.05, P ≤ 0.01, P ≤ 0.001, and P ≤ 0.0001. No control vs. control + JAB0505 comparisons were significant.

Techniques: Flow Cytometry, Muscles, Control, Comparison

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